1. Field of the Invention
This invention generally relates to medical procedures including the application of a pressure and, especially, to the field of vein grafting and preparation of a vein during vein grafting.
2. Description of Related Art
The first aortocoronary vein graft implantation in a human being was performed by Garrett and colleagues in May 1961. The subsequent pioneering work of Favaloro ushered in the era of surgical revascularization for the global epidemic of ischemic heart disease. Ironically, with the demonstration of the dramatic benefits obtainable by saphenous vein grafting came recognition of the ultimately palliative nature of the operation, due to the development of accelerated atherosclerosis within the saphenous vein conduits. During the first year after bypass surgery up to 15% of venous grafts occlude. In addition, between 1 and 6 years after bypass surgery the graft occlusion rate is 1% to 2% per year, and between 6 and 10 years the occlusion rate raise to 4% per year. By 10 years after surgery less than 60% of vein grafts are patent and only 50% of patent vein grafts are free of significant stenosis.
Reflecting this graft and native vessel patency rate, angina recurs in up to 20% of patients during the first year after bypass surgery using saphenous vein grafting and in 4% of patients annually during the ensuing 5 years. Further revascularization, either reoperative bypass surgery or percutaneous intervention, is required in 4% of patients by 5 years, 19% of patients by 10 years, and 31% of patients by 12 years after initial bypass surgery.
“Saphenous vein graft disease” is composed of three discrete processes: thrombosis, intimal hyperplasia, and atherosclerosis. These processes, although more or less temporally distinct, are interlinked pathophysiologically in the evolution of vein graft disease. Between 3% and 12% of saphenous vein grafts occlude, with or without symptoms, within the first month after bypass surgery. At this early stage, the principal underlying mechanism is graft thrombosis caused by a combination of alterations in the vessel wall, changes in blood rheology, and altered flow dynamics, as classically defined in Virchow's triad.
Even when performed under optimal conditions, the harvesting of venous conduits is associated with focal endothelial disruption. In particular, the high pressure distension used to overcome venospasm and to reveal reliably all unsecured side branches during harvesting causes prominent endothelial cell loss and medial damage. It was found that even the most skillful practitioner could not readily detect the relatively high pressures (600 to 700 mm Hg) generated by the syringe during harvesting, because a vein in spasm has a small diameter and allows wall tension (as defined by Laplace's Law).
Loss of the endothelial monolayer results in the accumulation of fibrin on the luminal surface, the adherence of platelets and neutrophils and a reduction in tissue plasminogen activator (tPA) production. Endothelial loss also activates the extrinsic coagulation cascade by tissue factor that is constitutively expressed in the exposed subendothelium. Tissue factor is also expressed, within 2 hours of initiating cardiopulmonary bypass, on the surfaces of endothelial cells activated by inflammatory cytokines.
In addition, saphenous veins, particularly when denuded, are highly sensitive to circulating vasoconstrictors, including the most potent endogenous vasoconstrictor, endothelin. The circulating concentration of endothelin-1 shows a marked initial rise, followed by an additional slower increment, after the onset of cardiopulmonary bypass and the resulting venoconstriction response may further attenuate flow and promote stasis.
Therefore a need exists to overcome the problems with the prior art as discussed above, and particularly for a way to more efficiently harvest saphenous veins so as to avoid increased pressure within the vein during the vein distention procedure.